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Objective <p>Tumour cells in a hypoxic state are more invasive, have stronger self-renewal capabilities, and are difficult to treat because of their ability to promote tumour recurrence and metastasis. The glycolysis inhibitor 3-bromopyruvic acid (3-BrPA) can completely inactivate glycolytic enzymes at extremely low drug concentrations, thereby exerting a strong inhibitory effect on the glucose energy metabolism of tumor cells. Therefore, we tested the inhibitory effect of 3-BrPA on hepatocellular carcinoma cells (HepG2) in vitro; then, we used the VX2 liver cancer model to study the antitumour effect of 3-BrPA combined with interventional embolization on liver cancer.</p> Methods <p>In vitro, a CCK-8 assay was used to detect the inhibitory effect of different concentrations of 3-BrPA on HepG2 cells, and light microscopy confirmed that the HepG2 cells were completely dead. Western blotting was used to detect the expression of key proteins involved in apoptosis. A total of 30 New Zealand white rabbits were used to establish a liver cancer model and were randomly divided into 3 groups 2&#xa0;weeks after tumor establishment: the control group was perfused with saline in the hepatic artery; the transcatheter arterial embolization (TAE) group was given TAE; and the experimental group was perfused with 3-BrPA combined with TAE. The tumor-bearing rabbits were killed one week after surgery. The tumor volume and tumor necrosis ratio were calculated via the histopathological examination.</p> Results <p>In vitro, the inhibitory effect of 3-BrPA on HepG2 cells increased with increasing concentration. 3-BrPA (100&#xa0;μmol/L) could induce the necrosis of HepG2 cells. Stimulation with 50&#xa0;μmol/L 3-BrPA could activate the tumor cell apoptosis pathway. 3-BrPA combined with TAE treatment could significantly inhibit tumor growth and cause more complete tumor necrosis.</p> Conclusion <p>3-BrPA not only has antitumour effects in vitro but can also significantly improve antitumour effects in the hypoxic microenvironment after embolization in vivo.</p>

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Targeting Glycolytic Enzymes with 3-Bromopyruvic Acid to Enhance the Efficacy of Interventional Embolization in Hepatocellular Carcinoma

  • 期刊论文

  • 发表日期：

    2025年2月21日

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  • Min Wang,
  • Xiao-ning Wu,
  • Xu Cheng,
  • Xiao-peng Guo,
  • Zhuang-lin Zeng,
  • Song-lin Song,
  • Ai-ping Cheng

摘要

Objective

Tumour cells in a hypoxic state are more invasive, have stronger self-renewal capabilities, and are difficult to treat because of their ability to promote tumour recurrence and metastasis. The glycolysis inhibitor 3-bromopyruvic acid (3-BrPA) can completely inactivate glycolytic enzymes at extremely low drug concentrations, thereby exerting a strong inhibitory effect on the glucose energy metabolism of tumor cells. Therefore, we tested the inhibitory effect of 3-BrPA on hepatocellular carcinoma cells (HepG2) in vitro; then, we used the VX2 liver cancer model to study the antitumour effect of 3-BrPA combined with interventional embolization on liver cancer.

Methods

In vitro, a CCK-8 assay was used to detect the inhibitory effect of different concentrations of 3-BrPA on HepG2 cells, and light microscopy confirmed that the HepG2 cells were completely dead. Western blotting was used to detect the expression of key proteins involved in apoptosis. A total of 30 New Zealand white rabbits were used to establish a liver cancer model and were randomly divided into 3 groups 2 weeks after tumor establishment: the control group was perfused with saline in the hepatic artery; the transcatheter arterial embolization (TAE) group was given TAE; and the experimental group was perfused with 3-BrPA combined with TAE. The tumor-bearing rabbits were killed one week after surgery. The tumor volume and tumor necrosis ratio were calculated via the histopathological examination.

Results

In vitro, the inhibitory effect of 3-BrPA on HepG2 cells increased with increasing concentration. 3-BrPA (100 μmol/L) could induce the necrosis of HepG2 cells. Stimulation with 50 μmol/L 3-BrPA could activate the tumor cell apoptosis pathway. 3-BrPA combined with TAE treatment could significantly inhibit tumor growth and cause more complete tumor necrosis.

Conclusion

3-BrPA not only has antitumour effects in vitro but can also significantly improve antitumour effects in the hypoxic microenvironment after embolization in vivo.